Effectors recruited to the inflammasome complex, such as caspase-1 and caspase-8, prompt strikingly similar downstream signaling. Cross-talk between caspase-3 and caspase-1 or -8 following inflammasome activation can induce apoptosis. Through inflammasome-mediated caspase-1 or caspase-8 cleavage of Bid, some studies have suggested that inflammasomes can initiate BAK and BAX signaling to activate caspase-3 to bring about apoptosis. Caspase-8 has also been shown to directly cleave GSDMD, thus curtailing apoptosis to induce pyroptosis. Furthermore, when activated by caspase-1 or caspase-8, caspase-3 can cleave GSDME to release N-terminal pores and initiate pyroptosis. Activated GSDMD and GSDME may also directly target mitochondrial membranes to induce a non-canonical mitochondrial apoptosis that results in apoptosome formation, and hence initiate a feedback caspase-3 amplification loop. It should be noted that in commonly studied inflammasome-responsive cell types, such as macrophages, the primary cell death observed from inflammasome sensor engagement is caspase-1-driven GSDMD activation and pyroptosis. However, alternate cell death pathways are often engaged upon (i) prolonged inflammasome signaling, (ii) reduced levels of activating stimuli (e.g. a lower level of cytosolic DNA has been shown to engage AIM2-mediated caspase-8 activation and apoptosis), or (iii) altered levels of relevant cell death effectors, such as loss, or reduced expression, of caspase-1 or GSDMD.